RÉSUMÉ
BACKGROUND: Disseminated intravascular coagulation (DIC) contributes to poor outcome in the early phase of trauma. We aimed to analyze and compare the prognostic performances of the International Society on Thrombosis and Hemostasis (ISTH) and the Korean Society on Thrombosis and Hemostasis (KSTH) scores in the early phase of trauma. METHODS: Receiver operating characteristics analysis was used to examine the prognostic performance of both scores, and multivariate analysis was used to estimate the prognostic impact of the ISTH and KSTH scores in the early phase of trauma. The primary outcome was 24-hour mortality and the secondary outcome was massive transfusion. RESULTS: Of 1,229 patients included in the study, the 24-hour mortality rate was 7.6% (n = 93), and 8.1% (n = 99) of patients who received massive transfusions. The area under the curves (AUCs) of the KSTH and ISTH scores for 24-hour mortality were 0.784 (95% confidence interval [CI], 0.760–0.807) and 0.744 (95% CI, 0.718–0.768), respectively. The AUC of KSTH and ISTH scores for massive transfusion were 0.758 (95% CI, 0.734–0.782) and 0.646 (95% CI, 0.619–0.673), respectively. The AUCs of the KSTH score was significantly different from those of the ISTH score. Overt DIC according to KSTH criteria only, was independently associated with 24-hour mortality (odds ratio [OR], 2.630; 95% CI, 1.456–4.752). Only the KSTH score was independently associated with massive transfusion (OR, 1.563; 95% CI, 1.182–2.068). CONCLUSION: The KSTH score demonstrates a better prognostic performance for outcomes than the ISTH score in the early phase of trauma.
Sujet(s)
Humains , Aire sous la courbe , Dacarbazine , Coagulation intravasculaire disséminée , Hémostase , Mortalité , Analyse multifactorielle , Pronostic , Courbe ROC , ThromboseRÉSUMÉ
PURPOSE: Evidence exists that dysregulation of Bcl-2 family members is involved in the pathogenesis of cancer development. The aim of this study was to explore whether the somatic mutation of proapoptotic Bcl-2 member genes, one of the mechanisms that prolong the survival of cancer cells, is involved in gastric carcinogenesis. MATERIALS AND METHODS: In the current study, to detect somatic mutations of the DNA sequences encoding the Bcl-2 homology 3 (BH3) domain of the human BAD, BIM, BIK, and Bcl-G genes in 60 advanced gastric adenocarcinomas, we used the polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP), and DNA sequencing. RESULTS: The SSCP analysis revealed no mutations in the coding regions of the BH3 domain in the cancers. CONCLUSION: The data presented here indicate that proapoptotic Bcl-2 member genes, BAD, BIM, BIK, and Bcl-G, may not be mutated in human gastric carcinomas and suggest that these genes might be altered by mechanisms other mechanisms somatic mutation.
Sujet(s)
Humains , Adénocarcinome , Apoptose , Séquence nucléotidique , Carcinogenèse , Codage clinique , Réaction de polymérisation en chaîne , Polymorphisme de conformation simple brin , Analyse de séquence d'ADNRÉSUMÉ
Recently, the -160 C/A polymorphism, located within the regulatory region of E-cadherin promoter, has been shown to influence E-cadherin transcription by altering transcription factor binding. We examined the effect of this polymorphism on risk of gastric cancer and on histological classification of intestinal- and diffuse-type gastric cancer in 146 normal healthy individuals and 292 Korean gastric cancer patients. Genomic DNA samples were examined by polymerase chain reaction (PCR)-single strand conformational polymorphism (SSCP)-sequencing and confirmed by restriction fragment length polymorphism (RFLP). Unexpectedly, there was no significant difference in the genotype frequencies of the polymorphism between normal control and gastric cancer patients (x(2) test, p=0.433). The estimated odd ratio of C/C to A/A genotype in gastric cancer cases was 1.07 (95% confidence interval, 0.396-2.870). We also found no evidence for differences in risk for the intestinal- and diffuse-type gastric cancer. These results suggest that the -160 C/A polymorphism of the E-cadherin has no direct effect on the risk of Korean gastric cancer development and on its histological classification.